INTRODUCTION
This report describes the history and clinical and post-mortem findings of a case of onion poisoning diagnosed in cattle in the Jerilderie area in June, 1980. Onions (Allium cepa) are grown by four producers at Jerilderie, with a total of approximately 1,200 acres being grown annually. It has been common practice in the past to feed second quality onions to stock as a convenient and cheap means of disposal. Prior to 1980 no losses have occurred in stock fed on onions and sheep in particular appear to thrive on them.
Onion poisoning has previously been described in the USA in cattle (Koger, 1956) and horses (Thorp and Harshfield, 1939). Koger (1956) described the usual signs of poisoning in cattle as being haemoglobinuria anaemia and icterus, with prompt recovery following a change of feed.
HISTORY
Poisoning occurred in a mob of 18 shorthorn cows and 1 bull, with 12 calves at foot. They were grazing on short, dry pasture of fairly poor quality, with access to (a) rice stubble. The cattle were given ad lib. access to onions for about 2 weeks prior to poisoning occurring. On 6th June the 6 year old bull was found dead and 6 cows and 2 calves were showing signs of severe depression, weakness and reluctance to move.
CLINICAL AND POST-MORTEM FINDINGS
Affected animals showed varying degrees of depression, and generally appeared weak and reluctant to move. Further examination was impossible due to distance from suitable facilities. Recovery was fairly rapid following removal from the onions.
Post-mortem examination was carried out on the bull and a range of specimens submitted for histopathology. The carcase was in fat condition and had a very strong smell of onions when opened.
The general appearance on post-mortem was one of an acute haemolytic crisis. The blood was very dark in colour, thin and watery and slow to clot. There was a severe haemoglobinuria and the kidney cortices had a dark, mottled appearance. Pericardial fluid was blood tinged and there was some petechiation of the epicardium. Jaundice was not a noticeable feature.
The rumen contained large quantities of onions, roughage and some rice seeds. There was haemorrhage and ulceration in the abomasal mucosa and the abomasum contained a large volume of watery brown fluid, while the intestinal contents were very thick and mucoid.
HISTOPATHOLOGY
Histopathology was carried out at RVL Wagga. The main findings reported were haemoglobinuric nephrosis, hepatic periacinar necrosis and splenic haemosiderosis, indicative of a haemolytic anaemia.
DISCUSSION
The findings observed in this case fit well with those reported previously (Koger 1956, Thorp and Harshfield, 1939). Illness and death are the result of a haemolytic anaemia, caused by the ingestion of toxic onions. The toxic element in the onions is thought to be N-propyl di sulphide and is similar to that causing anaemia in cases of Brassica poisoning (Smith 1980).
In this case the absence of noticeable jaundice in the dead animal could well be explained by the very rapid course of the disease, with a sudden haemolytic crisis resulting in rapid death before the development of jaundice. Surviving animals were not closely examined until they had recovered fully. Jaundice, subcutaneous oedema and depression were the main symptoms noted in a similar case occurring 2 months previously on a nearby property. Affected cows in this case were examined 4-5 days after the onset of poisoning.
Onion toxicity would appear to vary considerably, as there has been no problem with poisoning prior to 1980, although many cattle have been fed onions under similar conditions previously. Other cattle were also fed onions during 1980 with no apparent effect and some sheep in the area grow fat on a diet consisting almost exclusively of onions. Koger (1956) reports that no losses occurred in sheep maintained almost entirely on onions, during a period when numerous losses occurred in cattle. It would appear from this and from observations at Jerilderie that sheep are less susceptible to poisoning from onions than are cattle.
Why variations in toxicity for cattle occur is not known. And there were no changes in onion variety or treatment of the crop during 1980 which might explain the sudden appearance of toxicity.
References
Koger, L.M. (1956) J. Am. Vet. Med. Assoc. 129:75
Smith, R.H. (1980) Vet. Rec. 107:12-15
Thorp, Frank Jr. and Harshfield (1939) J. Am. Vet. Med. Assoc. 94:52-53